Podcast
Questions and Answers
A researcher is investigating potential therapeutic targets to enhance insulin secretion in patients with type 2 diabetes. Which of the following strategies would be LEAST effective in directly promoting insulin release from pancreatic beta cells?
A researcher is investigating potential therapeutic targets to enhance insulin secretion in patients with type 2 diabetes. Which of the following strategies would be LEAST effective in directly promoting insulin release from pancreatic beta cells?
- Increasing the activity of epinephrine on pancreatic beta cells. (correct)
- Administering a drug that mimics the action of GLP-1, thereby activating its receptor on beta cells.
- Introducing an agent that blocks the action of somatostatin on pancreatic islet cells.
- Developing a compound that directly inhibits ATP-sensitive potassium channels in the beta cell membrane.
A patient presents with a rare genetic mutation that impairs the function of GLUT-2 transporters in pancreatic beta cells, but not in other tissues. How would this mutation MOST directly affect glucose-stimulated insulin secretion?
A patient presents with a rare genetic mutation that impairs the function of GLUT-2 transporters in pancreatic beta cells, but not in other tissues. How would this mutation MOST directly affect glucose-stimulated insulin secretion?
- It would decrease the production of ATP within the beta cell mitochondria. (correct)
- It would prevent the depolarization of the beta cell membrane.
- It would increase the rate of glucose transport into the beta cell, leading to hyperinsulinemia.
- It would directly impair the exocytosis of insulin granules from the beta cell.
In an experiment, isolated pancreatic islets are exposed to varying concentrations of glucose. Which alteration would MOST directly impair the ability of increased intracellular calcium to stimulate insulin secretion?
In an experiment, isolated pancreatic islets are exposed to varying concentrations of glucose. Which alteration would MOST directly impair the ability of increased intracellular calcium to stimulate insulin secretion?
- Inhibiting the fusion of insulin-containing vesicles with the plasma membrane. (correct)
- Blocking L-type calcium channels on the beta cell membrane.
- Reducing the activity of glucokinase, the enzyme that phosphorylates glucose in the beta cell.
- Enhancing the activity of phosphodiesterases that degrade cAMP.
A research team discovers a novel compound that selectively enhances the activity of intestinal K cells in the duodenum. Based on the known physiology of these cells, what downstream effect would be MOST likely to occur?
A research team discovers a novel compound that selectively enhances the activity of intestinal K cells in the duodenum. Based on the known physiology of these cells, what downstream effect would be MOST likely to occur?
A scientist is investigating the effects of different nutrients on GLP-1 secretion. Which of the following dietary manipulations would be MOST effective in stimulating the release of GLP-1 from intestinal L cells?
A scientist is investigating the effects of different nutrients on GLP-1 secretion. Which of the following dietary manipulations would be MOST effective in stimulating the release of GLP-1 from intestinal L cells?
In a scenario of prolonged fasting, which hormonal response would be least likely to occur?
In a scenario of prolonged fasting, which hormonal response would be least likely to occur?
How does somatostatin (SST) influence glucose metabolism when nutrient availability is high?
How does somatostatin (SST) influence glucose metabolism when nutrient availability is high?
Which of the following describes the primary mechanism through which growth hormone (GH) increases glucose production?
Which of the following describes the primary mechanism through which growth hormone (GH) increases glucose production?
In the context of lipid metabolism, how do hormones like epinephrine and cortisol contribute to energy availability during stress?
In the context of lipid metabolism, how do hormones like epinephrine and cortisol contribute to energy availability during stress?
How do gut hormones, such as GLP-1 and GIP, influence insulin secretion and glucose homeostasis?
How do gut hormones, such as GLP-1 and GIP, influence insulin secretion and glucose homeostasis?
What is the differential impact of T3 and T4 from the thyroid on metabolic rate at the cellular level?
What is the differential impact of T3 and T4 from the thyroid on metabolic rate at the cellular level?
How do adipokines, specifically leptin and adiponectin, affect insulin sensitivity and glucose levels?
How do adipokines, specifically leptin and adiponectin, affect insulin sensitivity and glucose levels?
How does the interplay between insulin and glucagon influence metabolic processes differently in the liver, skeletal muscle, and adipose tissue?
How does the interplay between insulin and glucagon influence metabolic processes differently in the liver, skeletal muscle, and adipose tissue?
Considering the coordinated actions of insulin in various tissues, which of the following metabolic profiles would be expected in an individual with insulin resistance, where tissues exhibit a reduced response to insulin?
Considering the coordinated actions of insulin in various tissues, which of the following metabolic profiles would be expected in an individual with insulin resistance, where tissues exhibit a reduced response to insulin?
If a researcher is developing a novel drug to enhance insulin sensitivity, which of the following mechanisms would be the MOST promising target for achieving this therapeutic goal?
If a researcher is developing a novel drug to enhance insulin sensitivity, which of the following mechanisms would be the MOST promising target for achieving this therapeutic goal?
Following a high-carbohydrate meal, what intracellular event in a pancreatic beta cell is MOST directly responsible for triggering the exocytosis of insulin-containing granules?
Following a high-carbohydrate meal, what intracellular event in a pancreatic beta cell is MOST directly responsible for triggering the exocytosis of insulin-containing granules?
Which of the following scenarios would MOST directly impair the ability of insulin to stimulate glucose uptake in skeletal muscle?
Which of the following scenarios would MOST directly impair the ability of insulin to stimulate glucose uptake in skeletal muscle?
A patient with a pancreatic tumor that selectively secretes excessive amounts of somatostatin is likely to exhibit which of the following hormonal and metabolic abnormalities?
A patient with a pancreatic tumor that selectively secretes excessive amounts of somatostatin is likely to exhibit which of the following hormonal and metabolic abnormalities?
In a patient with liver cirrhosis, the liver's capacity to synthesize glycogen is significantly reduced. After a carbohydrate-rich meal, which of the following hormonal responses would be MOST crucial for maintaining blood glucose homeostasis in this patient?
In a patient with liver cirrhosis, the liver's capacity to synthesize glycogen is significantly reduced. After a carbohydrate-rich meal, which of the following hormonal responses would be MOST crucial for maintaining blood glucose homeostasis in this patient?
Which of the following best describes the functional relationship between insulin and C-peptide in the context of insulin synthesis and secretion?
Which of the following best describes the functional relationship between insulin and C-peptide in the context of insulin synthesis and secretion?
How does insulin orchestrate the coordinated regulation of glucose metabolism in both the liver and skeletal muscle to promote glucose homeostasis?
How does insulin orchestrate the coordinated regulation of glucose metabolism in both the liver and skeletal muscle to promote glucose homeostasis?
A novel drug is designed to specifically inhibit the enzyme phosphorylase in the liver. What effect would this drug have on blood glucose levels and glycogen metabolism, and how would the body likely compensate?
A novel drug is designed to specifically inhibit the enzyme phosphorylase in the liver. What effect would this drug have on blood glucose levels and glycogen metabolism, and how would the body likely compensate?
A researcher is investigating the effects of a novel compound on insulin signaling in adipocytes. The compound increases glucose uptake but inhibits glycerol phosphate synthesis. What downstream metabolic consequences are MOST likely to occur in these adipocytes?
A researcher is investigating the effects of a novel compound on insulin signaling in adipocytes. The compound increases glucose uptake but inhibits glycerol phosphate synthesis. What downstream metabolic consequences are MOST likely to occur in these adipocytes?
A patient has a mutation that impairs the function of the SNAT-2 transporter in skeletal muscle. How will this mutation MOST directly impact the patient's response to insulin?
A patient has a mutation that impairs the function of the SNAT-2 transporter in skeletal muscle. How will this mutation MOST directly impact the patient's response to insulin?
In an experiment, isolated hepatocytes are treated with a drug that selectively blocks the অ্যাক্টিভেশন of PI3 kinase. How does this treatment MOST directly affect insulin's actions in these cells?
In an experiment, isolated hepatocytes are treated with a drug that selectively blocks the অ্যাক্টিভেশন of PI3 kinase. How does this treatment MOST directly affect insulin's actions in these cells?
Following prolonged starvation, the body undergoes several hormonal and metabolic adaptations. Which of the following hormonal changes would be expected to have the MOST significant impact on maintaining blood glucose levels during this period?
Following prolonged starvation, the body undergoes several hormonal and metabolic adaptations. Which of the following hormonal changes would be expected to have the MOST significant impact on maintaining blood glucose levels during this period?
A researcher discovers a novel hormone that, when secreted, reduces the expression of hepatic glucokinase, an enzyme that phosphorylates glucose, trapping it within liver cells. What effect would the secretion of this hormone have on overall glucose homeostasis?
A researcher discovers a novel hormone that, when secreted, reduces the expression of hepatic glucokinase, an enzyme that phosphorylates glucose, trapping it within liver cells. What effect would the secretion of this hormone have on overall glucose homeostasis?
Amylin, co-secreted with insulin from pancreatic beta cells, plays a role in glucose regulation. What is the MOST direct mechanism by which amylin contributes to postprandial glucose control?
Amylin, co-secreted with insulin from pancreatic beta cells, plays a role in glucose regulation. What is the MOST direct mechanism by which amylin contributes to postprandial glucose control?
Flashcards
GLUT-2
GLUT-2
Transports glucose into beta cells.
ATP in Beta Cells
ATP in Beta Cells
Inhibits potassium channels, causing cell depolarization and calcium influx.
GIP and GLP-1
GIP and GLP-1
Stimulate insulin secretion.
GIP Function
GIP Function
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GLP-1 Function
GLP-1 Function
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Glycogenesis?
Glycogenesis?
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Glycogenolysis?
Glycogenolysis?
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Glycolysis?
Glycolysis?
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Gluconeogenesis?
Gluconeogenesis?
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Adipogenesis?
Adipogenesis?
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Lipogenesis?
Lipogenesis?
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Lipolysis?
Lipolysis?
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Insulin
Insulin
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Hormones that Increase Glucose
Hormones that Increase Glucose
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Anabolic Function
Anabolic Function
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Catabolic Function
Catabolic Function
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Insulin's Anabolic Actions
Insulin's Anabolic Actions
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Glucagon's Catabolic Action
Glucagon's Catabolic Action
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Pancreatic Alpha Cells
Pancreatic Alpha Cells
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Pancreatic Beta Cells
Pancreatic Beta Cells
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Proinsulin
Proinsulin
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C-Peptide
C-Peptide
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Insulin's Major Function
Insulin's Major Function
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GLUT4 Transporter
GLUT4 Transporter
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Rapid Insulin Actions (seconds)
Rapid Insulin Actions (seconds)
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Intermediate Insulin Actions (minutes)
Intermediate Insulin Actions (minutes)
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Slow Insulin Actions (hours)
Slow Insulin Actions (hours)
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Insulin Action in the Liver
Insulin Action in the Liver
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Study Notes
- Hormones like insulin, glucagon, somatostatin, epinephrine, growth hormone, and cortisol play roles in metabolism.
- The hormones regulate glucose, protein, and fat metabolism.
- Gut hormones and nutrients control metabolism.
Definitions
- Glycogenesis: Glycogen formation.
- Glycogenolysis: Glycogen breakdown.
- Glycolysis: Glucose breakdown to pyruvate or lactate.
- Gluconeogenesis: Glucose generation from non-carbohydrate sources. "Neo" means new.
- Adipogenesis: Maturation of pre-adipocytes into adipocytes.
- Lipogenesis: Conversion of acetyl-CoA to fatty acids.
- Lipolysis: Breakdown of fat to release fatty acids.
Hormones Regulating Carbohydrate and Lipid Metabolism
| Gland | Hormone(s) | Net Effect | Site(s) of Action |
|---|---|---|---|
| Pancreas | Insulin | Glucose lipid storage | Liver, fat, muscle |
| Glucagon | Glucose production | Liver, fat, muscle | |
| Somatostatin (SST) | Regulates insulin/glucagon | Multiple | |
| Amylin | Inhibits glucagon | Multiple | |
| Pituitary | Growth Hormone | Glucose production | Liver |
| Adrenal Gland | Epinephrine, Cortisol | Increase glucose | Multiple |
| GI Tract | GLP-1, GIP, Gastrin, Secretin, CCK | Alters insulin secretion | Pancreas |
| Adipose Tissue | Leptin, Adiponectin, Resistin | Satiety, ↓ glucose, Insulin resistance | Brain, Multiple |
| Thyroid | T3, T4 | Regulate metabolism | All cells |
- GH: Growth Hormone
- GLP-1: Glucagon-like peptide-1
- GIP: Gastric inhibitory polypeptide
- CCK: Cholecystokinin
Hormones and Glucose Levels
- Cortisol, Growth Hormone, Glucagon, and Epinephrine increase plasma glucose.
Anabolic vs. Catabolic Functions
| Function | Hormones | Description |
|---|---|---|
| Anabolic | Insulin, Growth Hormone (protein) | Builds storage forms (protein, fat, glycogen) from smaller molecules |
| Catabolic | Glucagon, Epinephrine, Cortisol | Breaks down molecules to increase glucose for metabolic needs (ex: glycogen) |
- Insulin promotes synthesis of protein, triglycerides, and glycogen.
- Growth hormone is anabolic specifically for protein synthesis.
- Glucagon, epinephrine and cortisol are catabolic.
Pancreatic Islets and Insulin Synthesis
- Alpha cells produce glucagon.
- Beta cells produce insulin.
- Delta cells produce somatostatin.
- PP cells produce pancreatic polypeptides.
- Insulin is synthesized as proinsulin in the rough ER, then to the Golgi for storage.
- Insulin is a hydrophilic hormone.
- Proinsulin is cleaved into insulin and C-peptide.
- C-peptide has no biological activity but is measured to assess insulin levels (1:1 ratio).
- Real insulin has two chains connected by disulfide bonds.
Insulin Release
- Insulin granules release insulin upon increased plasma glucose.
- Increased glucose is the signal for insulin secretion.
- Insulin requires processing post-proinsulin.
- Insulin is anabolic.
Mechanism of Action of Insulin
- Insulin activates metabolic pathways.
- PI3 kinase is activated upon insulin binding, inserting GLUT4 into the cell membrane.
- Insulin promotes glycogen storage and protein synthesis which are anabolic functions.
- Transcriptional pathway regulates mRNA and protein synthesis.
- Mitogenic pathway (MAP kinase) regulates mitogenic effects.
- GLUT4 vesicles fuse with the membrane via PI3 kinase, allowing glucose to enter.
Speed of Insulin Action
| Speed | Time | Action |
|---|---|---|
| Rapid | Seconds | GLUT4 to membrane, potassium uptake |
| Intermediate | Minutes | Protein synthesis, activates glycolytic enzymes (glucose to pyruvate), activates glycogen synthase |
| Slow | Hours | Inhibits phosphorylase and gluconeogenic enzymes, increases mRNAs for lipogenic enzymes |
Key Points
- Insulin decreases glucose concentration.
- Insulin slowly synthesizes fat synthesis/storage enzymes.
- Insulin receptors have binding sites and a kinase component.
- GLUT4 transporters are pre-synthesized.
- Insulin promotes protein synthesis.
Physiological Functions of Insulin in Different Organs
| Organ | Insulin Action |
|---|---|
| Liver | Stimulates glucose uptake (metabolized/stored as glycogen), ↑ glycolysis, glycogen synthesis, lipid/protein synthesis |
| Fat Tissue | Synthesizes triglycerides |
| Skeletal Muscle | Synthesizes protein (amino acids), ↑ glucose uptake, ↑ glycogen synthesis, ↓ protein catabolism, ↓ gluconeogenesis (amino acids), ↑ ketone/potassium uptake |
- Stimuli for Insulin Release: Glucose and amino acids.
- Amylin: secreted with insulin, inhibits glucagon, decreases glucose concentration, slows gastric emptying, and increases satiety.
Insulin Actions in Fat Tissue (Adipose Tissue)
- Insulin binds to surface receptors, ↑ glucose entry (GLUT4), ↑ glycerol phosphate synthesis, activates lipoprotein lipase (LPL).
- LPL breaks down fat complexes in blood vessels.
- Increases long-chain fatty acid entry (FATP).
- Major effect: increases fatty acid synthesis and triglyceride deposition.
- Inhibits hormone-sensitive lipase (HSL).
- Increases potassium uptake.
Insulin Actions in Skeletal Muscle
- Insulin binds to receptors, ↑ amino acid uptake (SNAT-2) for protein synthesis, ↑ glucose uptake (GLUT-4), ↑ glycogen synthesis.
- Decreases protein catabolism.
- Decreases release of gluconeogenic amino acids.
- Increases ketone uptake.
- Increases potassium uptake.
Insulin Actions in the Liver
- Glucose uptake isn't insulin-dependent but needs a concentration gradient.
- Insulin increases glycolysis, glycogen synthesis, decreases gluconeogenesis/ketogenesis, and increases protein and lipid synthesis (anabolic).
Glucose Stimulated Insulin Secretion in Beta Cells
- Beta cells secrete insulin.
- Glucose uptake (GLUT-2) in beta cells.
- Glucose is phosphorylated and metabolized to pyruvate.
- Pyruvate is oxidized (ATP production).
- ATP inhibits potassium channels, leading to depolarization.
- Depolarization activates calcium channels, causing calcium influx.
- Calcium stimulates insulin granule fusion and release.
Factors Affecting Insulin Secretion
| Stimulators | Inhibitors |
|---|---|
| Glucose | Low potassium concentration |
| Amino acids | Somatostatin, Galanin |
| Beta-keto acids | Epinephrine, Norepinephrine |
| Glucagon | Propranolol, Diazoxide, Thiazide diuretics |
| Acetylcholine | |
| Intestinal hormones (GIP, GLP, etc.) | |
| Beta-adrenergic stimulators | |
| Sulfonylurea drugs |
GI Hormones that Stimulate Insulin
- GIP (Gastric Inhibitory Peptide/Glucose-dependent insulinotropic peptide):
- Produced by intestinal K cells (duodenum/jejunum).
- Released in response to fat and glucose (fat more inhibitory).
- Stimulates insulin secretion (presence of glucose), enhances fatty acid incorporation into triglycerides, stimulates LPL.
- Promotes beta cell proliferation and survival.
- GLP-1 (Glucagon-like peptide-1):
- Secreted by intestinal L cells (small bowel/colon).
- Released in response to amino acids, fiber, sweeteners, sugars, glucose, fatty acids.
- Stimulates insulin secretion (presence of glucose), reduces hypoglycemia.
- Inhibits gastric emptying, decreases food intake, inhibits glucagon.
- Protects beta cells from apoptosis, stimulates beta cell proliferation.
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Description
Explore the roles of hormones like insulin and glucagon in regulating glucose, protein, and fat metabolism. Understand processes like glycogenesis, lipolysis and gluconeogenesis. Learn about the net effects and sites of action of key hormones involved in metabolic control.
